Send to

Choose Destination
J Physiol. 1990 Mar;422:29-39.

Responses to changes in filling and contractility of indices of human left ventricular mechanical performance.

Author information

Academic Department of Cardiovascular Medicine, Charing Cross and Westminster Medical School, London.


1. Beat-by-beat indices of contractility for assessment of inotropic effects in a given subject were studied using pacing with beta-adrenergic blockade, in eight patients undergoing routine left heart catheterization. A catheter-tip manometer was sited in the left ventricle and an electromagnetic velocity transducer was mounted further back on the same catheter so that it was sited in the ascending aorta. 2. The maximum rate of rise of left ventricular pressure (dPLV/dtmax), and of aortic velocity (maximum acceleration, MA) and stroke volume (SV) were all obtained with this catheter. Filling effects were assessed by head-up to head-down tilt, inotropic effects by paced post-extrasystolic potentiation. 3. Tilt produced a mean increase in left ventricular end-diastolic pressure (PLVED) of 8.1 mmHg (P less than 0.05), dPLV/dtmax decreased 4.3% (n.s.), peak velocity (PV) increased 23% (P less than 0.05), MA increased 5.4% (n.s.), and SV increased 17.5% (P less than 0.05). Post-extrasystolic potentiation produced a mean decrease in PLVED of 2.8 mmHg (n.s.), dPLV/dtmax increased 35% (P less than 0.05), PV increased 14% (P less than 0.05), MA increased 55% (P less than 0.05), and SV increased 8.7% (n.s.). 4. There was no difference in response between patients with normal and patients with impaired left ventricular ejection fraction. 5. It is concluded that increased left ventricular filling increases stroke volume greatly (Starling effect) but does not affect dPLV/dtmax, which (together with MA) nevertheless responds markedly to increased contractility. dPLV/dtmax appears to be a volume-insensitive index of contractility in the intact human, whether ejection fraction is normal or impaired.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Wiley Icon for PubMed Central
Loading ...
Support Center